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目的通过研究亚低温对大鼠局灶性脑缺血再灌注后诱导型一氧化氮合酶(iNOS)表达和细胞凋亡的影响,探讨亚低温脑保护的可能机制。方法雄性SD大鼠54只随机分为假手术组、常温缺血组和亚低温组。线栓法制备大脑中动脉闭塞再灌注模型,于缺血后48h取脑组织,邻片行HE染色,检测各组不同脑区iNOS蛋白表达和细胞凋亡情况,免疫双重染色研究iNOS蛋白表达与细胞凋亡间的关系,同时行NO含量测定。结果常温缺血组皮质缺血半暗带(IP)区iNOS免疫反应较强,TUNEL阳性细胞也主要位于皮质IP区,免疫双重染色发现TUNEL阳性细胞中存在着iNOS蛋白表达。亚低温组IP区iNOS蛋白表达明显下调,NO产生减少,IP区细胞凋亡的数目也减少。结论亚低温可能通过抑制IP区iNOS蛋白表达,减少NO产生,阻遏细胞凋亡,从而起到脑保护作用。
Objective To investigate the effects of mild hypothermia on the expression of iNOS and apoptosis after focal cerebral ischemia-reperfusion in rats and to explore the possible mechanism of hypothermia in cerebral protection. Methods Fifty-four male Sprague-Dawley rats were randomly divided into sham operation group, warm ischemia group and mild hypothermia group. The model of middle cerebral artery occlusion and reperfusion was established by the method of thread occlusion. The brain tissue was taken 48h after ischemia, the expression of iNOS protein and apoptosis in different brain regions were detected by HE staining. The expression of iNOS protein and The relationship between apoptosis, simultaneous determination of NO content. Results The iNOS immunoreactivity in the ischemic penumbra zone (IP) of normal temperature was stronger and TUNEL positive cells were mainly located in the cortex IP area. Immunohistochemical double staining showed that there was iNOS protein expression in TUNEL positive cells. In the mild hypothermia group, iNOS protein expression was significantly down-regulated, NO production was decreased, and the number of apoptotic cells in IP zone was also decreased. Conclusion Mild hypothermia may play a neuroprotective effect by inhibiting the expression of iNOS protein in IP area, decreasing the production of NO and inhibiting the apoptosis of cells.